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Objective: Despite extensive research, the etiology of negative symptoms is not well understood. Preliminary findings are linking motor disturbances to negative symptom severity. We aimed to further the understanding to what extent motor movement preparation influences negative symptom severity., Methods: In a cohort of 31 subjects with schizophrenia and 20 control subjects we recorded the readiness potential amplitude over Cz during spontaneous movements of the right and left thumb. We further assessed negative and positive symptom severity (scale for the assessment of negative and positive symptoms) as well as neurological soft signs (NSS)., Results: In subjects with schizophrenia the severity of negative symptoms was best predicted by the readiness potential amplitude and the NSS subdomain motor coordination. The correlation between deficits in motor coordination and negative symptom severity was partially mediated by the readiness potential amplitude in subjects with schizophrenia., Conclusions: Deficits in motor processing are linked to negative symptom severity in schizophrenia. The readiness potential may represent a biological marker of these basal deficits. In combination with the assessment of NSS, the readiness potential may be a marker of the course of negative symptom severity and help clarifying interdependencies between (pre)frontal networks for action initiation and coordination, as well as negative symptoms., Competing Interests: Declaration of competing interest None., (Copyright © 2023 Elsevier B.V. All rights reserved.)

Background: Early visual impairments probably partially caused by impaired interactions between magnocellular (M) and parvocellular (P) pathways (M priming deficit), and disturbances of basic self-awareness or self-disorders (SDs) are core features of schizophrenia. The relationships between these features have not yet been studied. We hypothesized that the M priming was impaired in first-episode patients and that this deficit was associated with visual aspects of SDs., Aim: To investigate early visual processing in a sample of first-episode schizophrenia patients and to explore the relationships between M and P functioning and visual aspects of SDs addressed by the Examination of Anomalous Self-Experience (EASE) interview., Method: Nine stimulating conditions were used to investigate M and P pathways and their interaction in a pattern reversal visually evoked potential (VEP) paradigm. N80 at mixed M- and P-conditions was used to investigate magnocellular priming. Generators were analyzed using source localization (Brain Electrical Source Analysis software: BESA). VEPs of nineteen first-episode schizophrenia patients were compared to those of twenty matched healthy controls by a bootstrap resample procedure. Visual aspects of SDs were analyzed through a factor analysis to separate symptom clusters of derealization phenomena. Thereafter, the associations between the main factors and the N80 component were explored using linear mixed models., Results: Factor analyses separated two EASE factors ("distance to the world", and "intrusive world"). The N80 component was represented by a single dipole located in the occipital visual cortex. The bootstrap analysis yielded significant amplitude reductions and prolonged latencies in first-episode patients relative to controls in response to mixed M-P conditions, and normal amplitudes and latencies in response to isolated P- and M-biased stimulation. Exploratory analyses showed significant negative correlations between the N80 amplitude values at mixed M-P conditions and the EASE factor "distance to the world", i.e. relatively higher amplitudes in the patient group were associated with higher subjective perceived derealization ("distance to the world")., Conclusions: The early VEP component N80 evoked by mixed M-P conditions is assumed to be a correlate of M priming, and showed reduced amplitudes and longer latencies in first-episode patients. It probably reflects a hypoactivation of the M-pathway. The negative association between visual SDs (derealization phenomena characterized by visual experiences of being more distant to the world), and the M priming deficit was counterintuitive. It might indicate a dysregulated activity of the M-pathway in patients with SDs. Further research is needed to better understand this preliminary finding., (Copyright © 2014 Elsevier B.V. All rights reserved.)

Background: Visual impairments in schizophrenia have been suggested to be partly caused by early processing deficits of the magnocellular (M) pathway. This might include disturbed interactions between the M and parvocellular (P) pathways and especially impaired M priming, which can disturb highlighting of relevant information. Such disorders may result from neurodevelopmental irregularities, which are assumed to be substantially involved in schizophrenia. This study sought to test the hypothesis that M priming is impaired in schizophrenia. In order to elucidate this neurodevelopmental aspect, we investigated patients with different ages of schizophrenia onset. This provided a useful design to integrate visual information processing in a neurodevelopmental model of schizophrenia., Method: Nine stimulus conditions were used to investigate the M- and P-pathways and their interaction in a pattern reversal VEP paradigm. N80 generators were analyzed using source localization (Brain Electrical Source Analysis software: BESA). Forty schizophrenia patients (early-onset=19; adult-onset=21) were compared with age- and gender-matched healthy controls (early-onset controls=19; adult-onset controls=21). Hypotheses were tested using a bootstrap resampling procedure., Results: The N80 component was represented by a single dipole located in the occipital visual cortex. The bootstrap analysis yielded significant differences between early-onset schizophrenia patients and controls. We found lower amplitudes in response to mixed M-P conditions and normal amplitudes in response to isolated P- and M-biased stimulation. Concerning the latencies, significant differences were found between adult-onset subjects and their controls, with prolonged latencies for schizophrenia patients., Conclusions: The early VEP component N80 evoked by mixed M-P conditions is assumed to be a correlate of M priming and showed reduced amplitude in early-onset schizophrenic patients but not in adult-onset patients. These findings point towards an M priming deficit in early-onset patients and are compatible with a neurodevelopmental hypothesis of schizophrenia, probably reflecting asynchronies in brain maturational abnormalities occurring at different ages of illness onset., (Copyright © 2012 Elsevier B.V. All rights reserved.)

Objective: Cognitive-perceptive 'basic symptoms' are used complementary to ultra-high-risk criteria in order to predict onset of psychosis in the pre-psychotic phase. The aim was to investigate the prevalence of a broad selection of 'basic symptoms' in a representative general adolescent population sample (GPS; N=96) and to compare it with adolescents first admitted for early onset psychosis (EOP; N=87) or non-psychotic psychiatric disorders (NP; N=137)., Methods: Subjects were assessed with the Bonn Scale for the Assessment of Basic Symptoms (BSABS). Prevalence of at least one 'basic symptom' and mean numbers were compared across the three groups. Logistic regression was used to predict group membership by BSABS subscales; risk ratios were calculated to identify 'basic symptoms' which best discriminated between groups., Results: The prevalence of at least any one 'basic symptom' was 30.2% in GPS compared to 81% in NP and 96.5% in EOP. Correct classification of EOP when compared to GPS was high (94.0%) and lower when compared to NP (78.6%). Cognitive symptoms discriminated best between EOP and NP., Conclusion: Alike other prodromal- and psychotic-like experiences, 'basic symptoms' are prevalent in the general adolescent population, yet at a lower rate compared to EOP and NP. The usage of 'at least one basic symptom' as a screening criterion for youth at risk of developing a psychotic disorder is not recommended in the general population or in unselected psychiatrically ill adolescents. However, particularly cognitive 'basic symptoms' may be a valuable criteria to be included in future 'at risk' studies in adolescents.

The expected therapeutic effect of estrogen as an adjunct treatment to antipsychotics in women suffering from schizophrenia for relapse prevention was to be tested under real-life conditions. A multicenter, randomized, placebo-controlled, double-blind, cross-over study based on an A-B-A-B (and/or B-A-B-A) design was applied. Forty-six hypoestrogenic women with schizophrenia hospitalized for the first time or repeatedly were included in the study. Their average age was 37.9 and they had been suffering from schizophrenia for 8.4 years. During the drug treatment phases, they received a three-phase estrogen-gestagen combination drug (17beta-estradiol+norethisterone acetate) in addition to an antipsychotic drug. Significant effects of the adjuvant hormone replacement therapy on the estradiol levels could be observed, and high and low levels of estradiol prevailed in the active drug and placebo phases, respectively. We did not find any difference either in defined relapse events or in the psychopathology between estradiol replacement and placebo phases. Neither did the required antipsychotic doses or the tolerance data differ between the two phases. Thus, the results of our study do not confirm the hypothesis that a combined estradiol/antipsychotic therapy is superior to an antipsychotic monotherapy for relapse prevention.

Background: Low estrogen levels leading to an elevated rate of menstrual dysfunctions such as amenorrhea and irregular menstruation have been described in women with schizophrenia and have often been attributed to antipsychotic-induced hyperprolactinemia. However, there is some evidence that "hypoestrogenism" in schizophrenic women does not occur exclusively under medication with hyperprolactinemia-inducing antipsychotics. While the precise mechanism of low estrogen levels in schizophrenic women has not been elucidated yet, "hypoestrogenism" is of clinical relevance because estrogen seems to endow an antipsychotic-like effect in schizophrenia and thus positively affect the course of illness in schizophrenic women. In addition, low levels of estrogen might have a negative effect on bone mineral density and on the cardiovascular system., Methods: To test the "hypoestrogenism hypothesis", hormone levels in 75 women with schizophrenia diagnosed according to DSM-IV and ICD-10 were determined in the follicular, periovulatory, and luteal phases of the menstrual cycle. Levels of estradiol, prolactin, luteinizing hormone (LH), follicle-stimulating hormone (FSH), progesterone, and testosterone were assessed., Results: The serum levels of estradiol were generally reduced during the entire menstrual cycle compared to normal reference values. With low levels of LH over the entire cycle and of progesterone in the luteal phase, anovulatory cycles were assumed. Hypoestrogenism was found in about 60% of the patients in accordance with a strict definition (estradiol serum level below 30 pg/ml in the follicular phase and below 100 pg/ml in the periovulatory phase). To rule out a possible effect of hyperprolactinemia on the gonadal axis and a subsequent effect on estradiol levels from treatment with conventional ("typical") antipsychotics, serum estradiol levels of patients treated with certain atypical antipsychotics known to induce only a mild increase in prolactin, or no increase at all, were compared with those from patients treated with conventional antipsychotics. The data clearly indicate high prolactin levels in the latter, but low levels in the group treated with atypical antipsychotics. In both groups, however, low levels of estradiol compared to normal reference values were measured., Conclusions: The present findings provide evidence that hypoestrogenism in schizophrenia occurs in women with and without antipsychotic-induced hyperprolactinemia. Further research should be conducted to clarify the cause of hypoestrogenism in schizophrenic women and focus on possible clinical implications.